ITGA2B and Glanzmann thrombasthenia: Romaniuk et al. have shown that gal-1 binding to platelets and gal-1-induced platelet activation is reduced, but not abolished, by CD41 antibodies, and on platelets from patients with Glanzmann thrombasthenia, meaning that integrin αIIbβ3 might not be the only receptor for gal-1 on platelets [9].